Botswana’s late twentieth-century sexual order originated as an adaptation to education and labour migration.31 It was one consequence of the mobility that drove the Central African epidemic, evident in the initial infection of Karonga, in the roles of long-distance drivers and dusty border towns like Beitbridge, and in the migration routes to the Copperbelt or the Nchalo sugar estate in southern Malawi, where the annual incidence of new infections is reported to have reached a brief peak of 17.1 per cent during 1994–5. In Zimbabwe, prevalence at antenatal clinics in 2000 ranged from 26.8 per cent in rural locations to 53.9 per cent in commercial (farming and mining) settings, peaking at 70.7 per cent in Chiredzi, another sugar plantation area.32 HIV thus followed the pattern of the commercial economy, straddling the urban–rural divide that checked it in Ethiopia. In each Central African country there was a close relationship between patterns of infection and of oscillating labour migration. Botswana experienced rapid urbanisation – Gaborone’s population multiplied more than ten times between 1971 and 1997 – but nevertheless had higher rural than urban prevalence of HIV because its people held to a long tradition of maintaining separate homes in towns and the countryside, between which they had in the past oscillated at different seasons, a practice now facilitated by motor transport. In Zimbabwe a similar oscillating pattern had grown up in the colonial period as men maintained land rights and families in the communal reserves while working in mines and cities. This, it has been argued, raised rural HIV prevalence close to urban levels.33 Colonial Zambia had known a similar pattern of mobility, but its severe economic decline after 1974 made towns less attractive and travel to distant provinces more difficult, so that the urban–rural differential in HIV prevalence was wider than in Zimbabwe, although narrower than elsewhere. Malawi, a poorer country, initially had much higher levels of infection in Blantyre and Lilongwe than in the countryside, but the contrast narrowed during the 1990s, partly perhaps in the natural course of epidemic development but also because economic decline drove infected young people into the countryside.34
Botswana’s epidemic was fuelled also by ethnic and cultural homogeneity, facilitating social interaction, and by its new-found diamond wealth, which gave it the world’s highest economic growth rate during the last third of the twentieth century. Yet, as its citizens said, Botswana was ‘a rich country of poor people’, 47 per cent of them living below the poverty line in 1993–4. Such polarisation fostered both risk taking in the rich and vulnerability in the poor.35 In Karonga those first infected had been the more prosperous and educated, but as the epidemic developed it focused increasingly on the poor. A survey of mining and industrial workers in Zambia, Botswana, and South Africa in 2000–1 showed HIV prevalence ranging from 4.5 per cent among managers to 10.5 per cent among skilled workers and 18.3 per cent among the unskilled.36 In addition to driving women into vulnerable occupations, poverty fostered disease by weakening medical systems and putting treatment beyond the reach of the poor. Between 1980 and 2000 the number of notified tuberculosis cases in Zambia, Zimbabwe, and Malawi multiplied five times as a result of HIV infection and decaying health systems.37 Although sexually transmitted diseases declined during the early years of the HIV epidemic, owing to wider use of condoms and greater emphasis on treatment, they were increasingly supplemented by HSV-2, which spread in synergy with HIV to infect 40 per cent of sexually active men and 61 per cent of sexually active women in Ndola in 1997. The lack of male circumcision in Central Africa added to the risk of HIV infection. In Botswana, ironically, circumcision had largely been abandoned during the twentieth century.38
While the epidemics in Malawi, Zambia, Zimbabwe, and Botswana reached maturity during the late 1990s, those in Mozambique and Namibia were still explosive. In both countries the warfare of the 1980s appears to have checked the spread of HIV by obstructing normal mobility. In Mozambique a study in ten provincial capitals in 1987 found average adult prevalence of 3.2 per cent, while in Maputo, isolated on the southern coast, antenatal prevalence was still less than 1 per cent in 1990.39 In Namibia, similarly, only 4.2 per cent of pregnant women were infected in 1988–92, with one area of high prevalence (14 per cent) at Katima Mulilo in the Caprivi Strip, which was not only the headquarters of the South African army but a meeting point of long-distance transport routes from Angola, Zambia, Zimbabwe, Botswana, and Namibia, notorious for high levels of commercial sex. Once Namibia was assured independence in 1990, however, some 43,387 registered exiles returned, mostly from Angola and Zambia. Many may well have been infected, for in 1992–3 prevalence was 17.2 per cent among Namibian soldiers in the northern Ovamboland region, many of them previously based outside the country. During the mid 1990s Namibia suffered an explosive epidemic, antenatal prevalence rising from 4 per cent in 1992 to 21 per cent in 2001. The northern nuclei at Katima Mulilo and Oshakati (another transport focus) retained high levels, but so now did the capital at Windhoek and the main port at Walvis Bay. By 1996 Aids was Namibia’s largest single cause of death. A relatively wealthy African country with great mobility, extreme income inequality, little female opportunity, and high levels of sexually transmitted diseases, it had many of the same conditions for epidemic expansion as Botswana.40 Mozambique, by contrast, followed more the patterns of poor countries like Malawi and Tanzania, once its civil war ended in 1992. Many returning refugees were probably infected and especially high prevalence existed on the north-western border with Malawi and in the central region along the Zambezi valley, long garrisoned by heavily infected Zimbabwean and Mozambican troops. In Maputo, antenatal prevalence rose between 1994 and 2002 from 3 to 19 per cent.41
Meanwhile South Africa experienced the world’s largest epidemic, with perhaps 5.3 million infected people in 2003.42 Not only did the socio-economic structures of Apartheid make the country an almost perfect environment for HIV, but the beginning of the epidemic coincided with the township revolt of the mid 1980s and its peak took place a decade later during the transition to majority rule, which compelled ordinary people to concentrate on survival and distracted both the outgoing regime and its nationalist successor from making HIV their chief priority. Yet it would be naive to think that even the most vigorous, stable, and popular government could have protected South Africa from a major epidemic. A contrast is sometimes drawn with Thailand, where an epidemic also became established during the early 1990s but was contained by 1999 at an adult prevalence of 2.2 per cent, whereas South Africa’s was 19.9 per cent.43 Yet this is to ignore the totally different ways in which HIV struck the two countries. Thailand was the first seriously affected country in South-East Asia, with no established epidemic on its borders and a disease that first took root among core groups of drug users, sex workers, and their clients, who could be targeted with impressive energy.44 South Africa, by contrast, bordered a massive continental epidemic and, as will be seen, had no identifiable core group but a great diversity of cross-border contacts that can scarcely now be traced. Of course, better political leadership could have reduced the impact of HIV, but trying to prevent the extensive infection of South Africa would have been like sweeping back the ocean with a broom. Thanks to its uniquely long, asymptomatic incubation period, HIV-1 could probably never have been prevented from reaching epidemic proportions once established in a general heterosexual population. That happened not in South Africa but ten years earlier and 2,500 kilometres away in Kinshasa.
All this is clear from the way the South African epidemic began. The first diagnosed case, in 1982, was in a white, homosexual air steward who had probably contracted the disease in New York and died of the Pneumocystis carinii pneumonia common among American patients. ‘Gay plague hits South Africa’, the Johannesburg Star trumpeted.45 Blood specimens from 200 homosexual men in Johannesburg in 1983 later showed that 32 were already infected. Although homosexuality was technically illegal in South Africa and a taboo subject among respectable Afrikaners, clinics were opened at major hospitals, injecting drug users were screened (and found negative), patients organised their own protection and care, and by 1990 the homosexual epidemic was already levelling off. Of 308 Aids cases reported in South Africa by January 1990, 207 had been in homosexuals, 195 of them white.46 Their infection was not transferred to the general heterosexual population, for the strain of HIV-1 infecting